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Pathology-Cardio > Valvular diseases > Flashcards

Valvular diseases Flashcards

1
Q

when does a valve close?

A

when back-flow pressure is greater than chamber pressure

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2
Q

when does a valve open?

A

chamber pressure is greater than out-flow pressure

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3
Q

what does directional flow depend on?

A

competency of valves

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4
Q

which valves are subject to greater greater mechanical abrasions?

A

pulmonic and aortic

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5
Q

why is velocity through semilunar valves greater?

A

due to smaller openings and greater chamber pressures

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6
Q

mitral stenosis

A

•Rheumatic heart disease
•Remarkably well tolerated
•Atrial enlargement associated
with atrial fibrillation

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7
Q

aortic stenosis

A
  • Aging (senile calcification)
  • Biscuspid aortic valve
  • Rheumatic heart disease
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8
Q

mitral regurgitation

A

•Mitral valve prolapse
•Advanced stenosis (fish
mouth) - RHD
•Ruptured papillary muscle

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9
Q

aortic regurgitation

A
  • Advanced valvular distortions

* Syphilitic aortitis

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10
Q

what murmurs are heard in systole?

A

AS

MR

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11
Q

what murmurs are heard during diastole?

A

AR

MS

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12
Q

machinery murmur is

A

patent ductus arteriosus

-switches directions

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13
Q

what side of lesion is more significant?

A

left

-means increased pressures

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14
Q

why are aortic valves more significant than mitral?

A

-sudden decompensation of aortic valve leads to death
-syncope due to aortic stenosis presages sudden death
-stenosis leads to left ventricular hypertrophy
-significance due both to effects on systemic outflow and
coronary flow

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15
Q

“jet streams” are associated with

A

AS

  • can damage vessels
  • allow thrombosis and bacterial deposition
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16
Q

what cause left sided lesions?

A
  1. Mitral valve prolapse
  2. Aortic stenosis
    - congenital bicuspid valve
    - rheumatic fever (also mitral stenosis)
    - senile calcifications
  3. Congenital malformations – VSD
  4. Infectious endocarditis
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17
Q

what cause right sided lesions?

A
  1. congenital lesions
  2. intravenous drug use (infectious)
  3. systemic diseases (Lupus) – both right and left
    valvular lesions
  4. carcinoid syndrome
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18
Q

Aortic stenosis

A

-Tricuspid aortic valve>bicuspid>rheumatic fever
(10%)
-65/75/85 – 2/3/4
-Normal aging – calcification
-presents in 8-9th decade
-Rheumatic heart disease – most commonly presents
as aortic stenosis (tricuspid) in adults <70
-decreasing in recent years
-Valve replacement when cardiac output is
insufficient

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19
Q

AS: bicuspid aortic valve

A

-1-2% of population; 2X more common in males
-familial; autosomal dominant with variable
penetrance
-early calcification and stenosis of aortic valve
-“heaped up” calcifications interfere with function
-presents 6th – 7th decade
-calcification of tricuspid valve presents later
-progressive stenosis; late regurgitation

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20
Q

cardiac symptoms of Mitral valve prolapse

A

-mitral regurgitation (significant if greater than
15%)
-supraventricular arrhythmias/palpitations –
particularly with atrial enlargement secondary to
regurgitation
-sudden death
-bacterial endocarditis (no longer indication for
dental prophylaxis)

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21
Q

clinical findings with mitral valve prolapse?

A
  • mid to late systolic clicks
  • continuous or crescendo systolic murmur
  • syncope requires further investigation
22
Q

MVP syndrome/dysautonomia

A
  • chest pain, dyspnea, fatigue, dizziness, near syncope, anxiety,
  • life style modifications, education and re-assurance
23
Q

myxomatous degeneration with MVP

A

-excessive mucopolysaccharides, stretching of
valve leaflets
-genetic variants of fibrillin, elastin, and collagen
(Marfan’s, Ehler’s-Danlos)
-anorexia, dehydration in some women that is
reversible
-increased mitral valve surface area with
prolapse into left atrium during systole

24
Q

rheumatic heart disease

A
  • S. pyogenes
  • untreated strep pharyngitis in children
  • is main cause of death from heart disease in ages 5-25
  • associated with pharyngitis, PSGN, impetigo (GAS)
25
autoimmune reaction in rheumatic heart disease
-several weeks after severe pharyngitis -antibodies to hyaluronate in Strep capsules cross react with glycoproteins in heart valves -antibodies to streptolysin O good indicator of severity of disease -cross-reaction to streptolysin M; different M types may have different potential for RF -associated with specific HLA types
26
pathogenesis of rheumatic heart disease
-lesions sterile and do not result from direct bacterial invasion -rate of development increases with severity of the initial Strep infection -individual susceptibility may be related to genetically determined immune response genes to Strep antigens
27
acute rheumatic fever
1. Pancarditis -Myocarditis -Pericarditis -Valvular disease -Mitral valve > aortic valve -Valvular insufficiency; mitral insufficiency most commonly involved in acute heart failure
28
rheumatic fever: aschoff bodies
- pathognomonic of rheumatic fever - collections of reactive histiocytes - around blood vessels
29
rheumatic fever: anitschkow myocytes
- actually HISTIOCYTES - not limited to rheumatic fever: occur with any form of inflammation of heart - cardiac histiocytes - caterpillar chromatin pattern
30
what percent develops chronic valvular disease in rheumatic heart disease?
65-75% Chronic inflammatory reaction leading to fibrosis and thickening of valvular - stenosis -mitral > aortic >>>tricuspid -leads to fusion (2-10 years), stenosis +/- insufficiency -becomes clinically apparent after several decades -most common cause of mitral (99%); 10% of aortic stenosis
31
what clinical consequences result from chronic valvular disease?
include atrial enlargement with atrial fibrillation, LVH, systolic and diastolic murmur, hemolytic anemia, and pulmonary hypertension
32
bacterial endocarditis presentation
fever heart murmur fatigue
33
most common presentation of bacterial endocarditis
FEVER OF UNKNOWN ORIGIN
34
bacterial endocarditis: left sided emboli
1. Osler’s nodes 2. Janeway lesions 3. Brain abscesses 4. multiple right sided pulmonary emboli) - multiple blood cultures (negative in fungal) - long-term antibiotic therapy
35
organisms that can cause bacterial endocarditis
``` 95% bacteria 1.Strep 2.Viridans 3.Staph -enterococci -pneumococci -G- rods 5% rickettsia, chlamydia, fungal ```
36
predisposing conditions
- any anomaly leading to abnormal flow, shunting (particularly right to left through septal defects), exposure of collagen, or damage to valves (fibrin deposition) - IV drug use predisposes to right-sided infections (S. aureus, Candida, Aspergillus)
37
where does most endocarditis occur on?
left sided
38
acute endocarditis
-S. aureus -normal valves -can occur on right, especially with IV drug use (right>left) -high fever, new onset murmur -rapidly progressive lesions, very destructive -fenestrations, distortions -destructive lesions of aortic valve lead to sudden death
39
sub-acute endocarditis
S. viridans -abnormal valves -left>right (almost never on right) -low or no fever, new onset murmur, slowly progressive lesions -antibiotic prophylaxis for dental procedures and surgery only for prosthetic valves, previous endocarditis or specific congenital defects
40
IV drug use endocarditis
-Right > left or bilateral
41
organisms that cause endocarditis in IV drug users
- S. aureus most common - gram negatives or multiple (including Pseudomonas) - fungi - Candida, aspergillus
42
what are the vegetations seen in endocarditis?
-Mixture of bacteria, fibrin, thrombosis, inflammatory cells -Deposition on valve surface; enhanced by prior damage or NBTE -Local proliferation of bacteria -Structural damage with Staph aureus -Emboli to brain, peripheral circulation (Osler’s nodes, Janeway lesions) -Flow side; edge of cusps
43
non-bacterial thrombotic endocarditis
- Sterile lesions; no bacteria | - Deposition of platelets, thrombin
44
what is associated with NBTE
- SLE – Libman Sacks endocarditis - Cancer – pancreatic carcinoma (migrating thrombophlebitis) (pro-coagulant state)
45
SLE – Libman Sacks endocarditis
-vegetations on the mitral and tricuspid valves (NBTE) -occur in approximately half the cases of SLE -unlike rheumatic heart disease, often involves valves on the RIGHT side of the heart -composed of necrotic debris, fibrinoid material, disintegrating fibroblasts and inflammatory cells -small (usually 1-4 mm); usually occur on flow side of leaflets, but can occur behind them -dysfunction results in regurgitation -? associated with anti-phospholipid syndrome
46
which valves does Libman Sacks endocarditis usually involve?
right side of heart
47
Carcinoid tumors
-Neuroendocrine-derived tumor of the GI tract, lungs that secrete vaso-active substances (serotonin, kallikrein) -Flushing, diarrhea
48
where are Carcinoid tumors most common?
Most common site of involved primary tumor is in the small intestine (ileum) where it metastasizes to the liver (appendix more common, but doesn’t metastasize)
49
Carcinoid syndrome
-Valvular associated only with metastasis to liver and secretion of substances into the hepatic vein (to right heart and lungs) -affect only the right side of the heart – metabolized in the lung and never make it to the left side -Primarily thickening of the valve with various degrees of stenosis
50
in Carcinoid syndrome, which valve is most commonly affected?
tricuspid valve
51
artificial valves
``` -Valve replacement required for stenosis (M/A) or severe regurgitation (A) -Artificial or natural -Associated with thrombosis -Long-term anticoagulation -Associated with infection, including Staph epidermidis -Often need to be replaced ```

Pathology-Cardio (11 decks)

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